Ventilatory chemoreceptor response in parents of children at risk for sudden infant death syndrome.
We postulated that parents of infants who sustain near-death episodes associated with defective chemical regulation of breathing might share a similar defect. We, therefore, measured the ventilatory responses to progressive hypoxia and hypercapnia individually in eight sets of parents of infants who had sustained at least one near-death episode (apnea, cyanosis, pallor, limpness, and responsive only to mouth-to-mouth resuscitation); each infant had a ventilatory response to CO2 which was more than 2 S.D. below the mean normal. Ventilatory function measured by vital capacity forced expiratory volume 1.0 and flow curves was normal in each group. Responses to hypercapnia and hypoxemia in both fathers and mothers were similar to 11 pairs of controls. Ventilation during CO2 rebreathing normalized for surface area increased 0.87 liter/min/mm Hg in fathers, 0.94 in controls, 0.87 in mothers, and 0.75 in controls. Ventilation during progressive hypoxemia increased 88 liter/min/1 divided by mm Hg in fathers, 92 in controls, 86 in mothers, and 101 in controls. None of these differences was significant.
D000328:Adult; D002245:Carbon Dioxide / Q000494:pharmacology; D002628:Chemoreceptor Cells / Q000502:physiology*; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000150:complications; D008297:Male; D012119:Respiration; D012306:Risk; D013398:Sudden Infant Death / Q000209:etiology*
D002245:Carbon Dioxide